Y. U. Liang

Let an oracle be called low for prefix-free complexity on a set in case access to the oracle improves the prefix-free complexities of the members of the set at most by an additive constant. Let an oracle be called weakly low for prefix-free complexity on a set in case the oracle is low for prefix-free complexity on an infinite subset of the given set. Furthermore, let an oracle be called low and weakly for prefix-free complexity along a sequence in case the oracle is low and weakly low, respectively, for prefix-free complexity on the set of initial segments of the sequence. Our two main results are the following characterizations. An oracle is low for prefix-free complexity if and only if it is low for prefix-free complexity along some sequences if and only if it is low for prefix-free complexity along all sequences. An oracle is weakly low for prefix-free complexity if and only if it is weakly low for prefix-free complexity along some sequence if and only if it is weakly low for prefix-free complexity along almost all sequences. As a tool for proving these results, we show that prefix-free complexity differs from its expected value with respect to an oracle chosen uniformly at random at most by an additive constant, and that similar results hold for related notions such as a priori probability. Furthermore, we demonstrate that on every infinite set almost all oracles are weakly low but are not low for prefix-free complexity, while by Shoenfield absoluteness there is an infinite set on which uncountably many oracles are low for prefix-free complexity. Finally, we obtain no-gap results, introduce weakly low reducibility, or WLK-reducibility for short, and show that all its degrees except the greatest one are countable.

Tight control and multifactorial regulation of gene expression are important challenges in genetic engineering and are critical for the development of regulatory circuits. Meeting these challenges will facilitate transgene expression regulation and support the fine-tuning of metabolic pathways to avoid the accumulation of undesired intermediates. By employing the endoribonuclease Csy4 and its recognition sequence from Pseudomonas aeruginosa and manipulating 5'UTR of mRNA, we developed a two-component expression-repression system to tightly control synthesis of transgene products. We demonstrated that this regulatory device was functional in monocotyledonous and dicotyledonous plant species, and showed that it can be used to repress transgene expression by >400-fold and to synchronize transgene repression. In addition to tissue-specific transgene repression, this system offers stimuli-dependent expression control. Using a bioinformatics approach, we identified 54 orthologous systems from various bacteria, and then validated in planta the activity for a few of those systems, demonstrating the potential diversity of such a two-component repressor system.

Strong Turing Determinacy, or ${\mathrm {sTD}}$, is the statement that for every set A of reals, if $\forall x\exists y\geq _T x (y\in A)$, then there is a pointed set $P\subseteq A$. We prove the following consequences of Turing Determinacy ( ${\mathrm {TD}}$ ) and ${\mathrm {sTD}}$ over ${\mathrm {ZF}}$ —the Zermelo–Fraenkel axiomatic set theory without the Axiom of Choice: (1) ${\mathrm {ZF}}+{\mathrm {TD}}$ implies $\mathrm {wDC}_{\mathbb {R}}$ —a weaker version of $\mathrm {DC}_{\mathbb {R}}$.(2) ${\mathrm {ZF}}+{\mathrm {sTD}}$ implies that every set of reals is measurable and has Baire property.(3) ${\mathrm {ZF}}+{\mathrm {sTD}}$ implies that every uncountable set of reals has a perfect subset.(4) ${\mathrm {ZF}}+{\mathrm {sTD}}$ implies that for every set of reals A and every $\epsilon>0$ :(a)There is a closed set $F\subseteq A$ such that $\mathrm {Dim_H}(F)\geq \mathrm {Dim_H}(A)-\epsilon $, where $\mathrm {Dim_H}$ is the Hausdorff dimension.(b)There is a closed set $F\subseteq A$ such that $\mathrm {Dim_P}(F)\geq \mathrm {Dim_P}(A)-\epsilon $, where $\mathrm {Dim_P}$ is the packing dimension.